Protocols for Enhancing Function of Fetal Islets in vitro and following Transplantation (A. Hayek, G.M. Beattie). Expression of Two Nonallelic Reg Genes in the Developing Human Pancreas: Effects in vitro of Nicotinamide and Maternal Growth Factors (B. Formby et al.). Preparation of Fetal Islets for Transplantation: Importance of Growth Factors (D.A. Hullet et al.). Studies of Fetal Porcine Isletlike Cell Clusters-A Tissue Source for Xenotransplantation in Insulindependent Diabetes Mellitus? (S. Sandler). Basic Biology of Pig Fetal Pancreas and Its Use as an Allograft (B.E. Tuch et al.). Combined Transplantation of Adult and Fetal Islets for Improvement of Graft Function (Y. Mullen). Studies on Pretreatment of Human Fetal Islet in Vitro and Clinical Islet Transplantation in China (Y.F. Hu et al.). The Use of Human Fetal Islet Tissue for Adjunctive Treatment in Insulindependent Diabetic Patients: The Case for 'Partial Success' (L. JovanovicPeterson et al.). Longterm Studies with Cultured and Cryopreserved Human Fetal Islets for Islet Transplantation in Hungary (G. Farkas). Fetal Islet Transplantation and Pregnancy (C.M. Peterson et al.). Encapsulated Human Islet Transplant Trials in Type I Diabetic Patients (P. SoonShiong). 4 additional articles. Index.

Diabetic nephropathy is a tragic illness. Its often insidious onset in the insulin dependent (type I) diabetic, typically a young adult, heralds the last act in the course of a disease that will increasingly become the dominant preoccupation in the patient's shortened life. For most type II diabetics, the beginning of clinical renal insufficiency is but a phase in a continuous deterioration that affects the integrity ofjob, marriage, and family. The nephropathic diabetic is hypertensive, has worsening retinopathy, and more often than not, is also plagued by peripheral vascular insufficiency, heart disease, gastrointestinal malfunction, and deepening depression. Until the 1980's, few type I diabetics who became uremic (because ofdiabetic nephropathy) lived for more than two years. Hardly any attained true rehabilitation. This dismal prognosis is changing substantially for the better. Research in diabetes has resulted in striking advances at both ends of the type I diabetic's natural history. In one exciting clinical trial now underway in London, Ontario, halfofchildhood diabetics treated with cyclosporine within six weeks of onset evince"permanent" disappearanceofhyperglycemia and the need for insulin. At the otherendofthe natural historyofdiabetes for the nephropathic patientwith worsening eye disease (renal-retinal syndrome), who receives a kidney transplant, patient and graft survival, two years after cadaveric kidney transplantation in type I diabetics is now equal to that of the nondiabetic."

The breadth of research efforts represented by the many excellent papers in these proceedings is an eloquent testimonial to the idea of one man Dr. Josiah Brown-to whose memory this volume is dedicated. His tragic and unexpected loss in a swimming accident in August 1985 brought to an abrupt close a long and distinguished career as a physician and scientist. The possibility of using fetal pancreas tissue for transplantation into insulin-deficient diabetic recipients had intrigued Dr. Brown for several years prior to 1972, when he began in earnest to assemble a research team to explore this idea in detail. He felt that improvements in the formulation and administration of insulin (even the later recombinant human insulin) had taken us about as far as we could go in treating diabetes, and that methods for achieving complete cures must be explored. Numerous advantages of the fetal pancreas quickly became apparent, and were explored scientifically by Dr. Brown and his group. Transplanted pancreas tissue from a fetal donor of the appropriate developmental stage engrafts quickly, and can reverse diabetes very efficiently (1-3). By shunting the venous'drainage of the graft into the hepatic portal vein, a single pancreatic rudiment can, in time, provide enough insulin to restore normoglycemia and urine volume in a diabetic adult recipient (4). As with fetal pancreas rudiments in culture, transplanted fetal pancreas tissue loses its exocrine character, while continuing to develop and maintain endocrine function.